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Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway

Agents inhibiting microglial activation are attracting attention as candidate drugs for neuroprotection in neurodegenerative diseases. Recently, researchers have focused on the immunosuppression induced by rifampicin. Our previous study showed that rifampicin inhibits the production of lipopolysacch...

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Autores principales: BI, WEI, ZHU, LIHONG, JING, XIUNA, ZENG, ZHIFEN, LIANG, YANRAN, XU, ANDING, LIU, JUN, XIAO, SONGHUA, YANG, LIANHONG, SHI, QIAOYUN, GUO, LI, TAO, ENXIANG
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148376/
https://www.ncbi.nlm.nih.gov/pubmed/25119251
http://dx.doi.org/10.3892/mmr.2014.2480
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author BI, WEI
ZHU, LIHONG
JING, XIUNA
ZENG, ZHIFEN
LIANG, YANRAN
XU, ANDING
LIU, JUN
XIAO, SONGHUA
YANG, LIANHONG
SHI, QIAOYUN
GUO, LI
TAO, ENXIANG
author_facet BI, WEI
ZHU, LIHONG
JING, XIUNA
ZENG, ZHIFEN
LIANG, YANRAN
XU, ANDING
LIU, JUN
XIAO, SONGHUA
YANG, LIANHONG
SHI, QIAOYUN
GUO, LI
TAO, ENXIANG
author_sort BI, WEI
collection PubMed
description Agents inhibiting microglial activation are attracting attention as candidate drugs for neuroprotection in neurodegenerative diseases. Recently, researchers have focused on the immunosuppression induced by rifampicin. Our previous study showed that rifampicin inhibits the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators and improves neuron survival in inflammation; however, the mechanism through which rifampicin inhibits microglial inflammation and its neuroprotective effects are not completely understood. In this study, we examined the effects of rifampicin on morphological changes induced by LPS in murine microglial BV2 cells. Then we investigated, in BV2 microglia, the effects of rifampicin on two signaling pathway componentss stimulated by LPS, the Toll-like receptor-4 (TLR-4) and the nuclear factor-κB (NF-κB). In addition, we co-cultured BV2 microglia and neurons to observe the indirect neuroprotective effects of rifampicin. Rifampicin inhibited LPS-stimulated expression of the TLR-4 gene. When neurons were co-cultured with LPS-stimulated BV2 microglia, pre-treatment with rifampicin increased neuronal viability and reduced the number of apoptotic cells. Taken together, these findings suggest that rifampicin, with its anti-inflammatory properties, may be a promising agent for the treatment of neurodegenerative diseases.
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spelling pubmed-41483762014-08-29 Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway BI, WEI ZHU, LIHONG JING, XIUNA ZENG, ZHIFEN LIANG, YANRAN XU, ANDING LIU, JUN XIAO, SONGHUA YANG, LIANHONG SHI, QIAOYUN GUO, LI TAO, ENXIANG Mol Med Rep Articles Agents inhibiting microglial activation are attracting attention as candidate drugs for neuroprotection in neurodegenerative diseases. Recently, researchers have focused on the immunosuppression induced by rifampicin. Our previous study showed that rifampicin inhibits the production of lipopolysaccharide (LPS)-induced pro-inflammatory mediators and improves neuron survival in inflammation; however, the mechanism through which rifampicin inhibits microglial inflammation and its neuroprotective effects are not completely understood. In this study, we examined the effects of rifampicin on morphological changes induced by LPS in murine microglial BV2 cells. Then we investigated, in BV2 microglia, the effects of rifampicin on two signaling pathway componentss stimulated by LPS, the Toll-like receptor-4 (TLR-4) and the nuclear factor-κB (NF-κB). In addition, we co-cultured BV2 microglia and neurons to observe the indirect neuroprotective effects of rifampicin. Rifampicin inhibited LPS-stimulated expression of the TLR-4 gene. When neurons were co-cultured with LPS-stimulated BV2 microglia, pre-treatment with rifampicin increased neuronal viability and reduced the number of apoptotic cells. Taken together, these findings suggest that rifampicin, with its anti-inflammatory properties, may be a promising agent for the treatment of neurodegenerative diseases. D.A. Spandidos 2014-10 2014-08-11 /pmc/articles/PMC4148376/ /pubmed/25119251 http://dx.doi.org/10.3892/mmr.2014.2480 Text en Copyright © 2014, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
BI, WEI
ZHU, LIHONG
JING, XIUNA
ZENG, ZHIFEN
LIANG, YANRAN
XU, ANDING
LIU, JUN
XIAO, SONGHUA
YANG, LIANHONG
SHI, QIAOYUN
GUO, LI
TAO, ENXIANG
Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway
title Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway
title_full Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway
title_fullStr Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway
title_full_unstemmed Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway
title_short Rifampicin improves neuronal apoptosis in LPS-stimulated co-cultured BV2 cells through inhibition of the TLR-4 pathway
title_sort rifampicin improves neuronal apoptosis in lps-stimulated co-cultured bv2 cells through inhibition of the tlr-4 pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4148376/
https://www.ncbi.nlm.nih.gov/pubmed/25119251
http://dx.doi.org/10.3892/mmr.2014.2480
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